Dyslexia is a disorder in learning to read that often appears to have a congenital basis and is found more frequently in males than in females. It has been suggested that a prolonged or excessive surge of developmental testosterone may disrupt the development of the cerebral cortex and result in dyslexia. In the present proposal, this hypothesis is tested by using the rat as a model so that developmental hormone levels can be manipulated. Excess testosterone will be injected during postnatal development (days 2-8) when cortical neurons are migrating and differentiating. Three cortical areas (frontal, parietal, visual) will be sampled in weaning age males that have been injected with excess testosterone and in oil injected controls. The cortices will be examined through Nissl stains where the size of the cortical layers and soma size and density will be measured. The size of the dendritic tree as an indicator of synaptic connectivity will also be quantified in Golgi stained sections. It is hypothesized that exposure to an excess of testosterone will disrupt the organization of the cerebral cortex. This can serve as a model for what testosterone perturbations could effect in more subtle form during the development of the cortex in human dyslexics.